Keywords
pneumocephalus - nitrous oxide - postoperative complications - craniocerebral trauma
- skull - cerebrospinal fluid leak
Introduction
Usually, the postoperative sterile pneumocephalus is easily distinguishable on axial
imaging and clinical history from those associated with head trauma, spontaneous cerebrospinal
fluid (CSF) leaks, and intracranial infection with gas-producing species,[1]
[2]
[3]
[4] though at times combinations of these etiologies can contribute to challenging clinical
circumstances. Postoperative cranial imaging generally demonstrates one or more non-compressive
localized volumes of air that remain in the surgical bed, which are essentially self-limited
and resolve over several weeks or less. Unless a mass removed was large or the brain
had been chronically compressed (such as in a subdural hematoma), this collection
is small and is often localized to the subdural and/or extradural space, depending
on the dural closure technique used.
Resections performed in a dependent position, such as in sitting or prone posterior
fossa neurosurgery in the reverse Trendelenburg position, can allow CSF to drain out
of the cerebral convexities with a diffuse distribution of air in the basal cisterns,
cerebral sulci and fissures, and occasionally the ventricles. The imaging results
can be striking; however, the collections are generally benign. This air takes the
place of the CSF, which had been drained from the surgical field and is generally
low in total volume and non-compressive. In any approach, in the event of removal
of large masses or large compressive lesions, such as a subdural hematoma, the residual
air that fills the surgical void can be substantial if care is not taken to fill the
surgical cavity with surgical irrigation. In these cases, excessive hyperventilation
intraoperatively, particularly at the time of closure, can lead to collections under
mild pressure. Hydrostatic forces ensure these are rapidly absorbed into the circulation,
with typically transient brain compression of low concern.
On the other hand, in rare cases, pneumocephalus can develop or progress after a surgical
wound has been closed. This is generally associated with dural injuries, which create
one-way “ball-valves” in surrounding tissue (or with the use of positive pressure
ventilation acutely after endonasal skull base surgery or other surgical violations
of the anterior skull base[5]
[6]
[7]
[8]). In the event that the air collection is progressively pressurized beyond ambient
pressure, the term pressure or tension pneumocephalus is used, analogously to its
use in tension pneumothorax. This portends a potentially progressive and more morbid
condition.
The incidence and duration of postoperative and tension pneumocephalus have been studied.
In a study of 240 patients who underwent craniotomy or craniectomy, as expected, 100%
of patients had some degree of pneumocephalus on computed tomography (CT) imaging,
regardless of size or symptomatology, which was, in most cases, asymptomatic.[9] There was a 25% resolution of postoperative pneumocephalus within the first week.
At 2 weeks, 40.4% resolution occurred, and at 3 weeks, 73.6% resolution occurred.
In another case study of 54 patients with all causes of otogenic pneumocephalus, tension
pneumocephalus was present in 66% of cases, with trauma (36%) being the most common
etiologic factor, while otitis media (30%), otologic surgery (30%), and congenital
defects (2%) accounted for the remainder.[10]
Generally, all patients with tension pneumocephalus or a persistent CSF leak will
require revision surgery to repair the dural violation and potentially the underlying
cause of the dural or surgical closure defect, and at times can have a protracted
clinical course. Three illustrative case reports demonstrate the breadth of techniques
required in the surgical and critical care management of these findings, with each
demonstrating unique challenges that both surgeons and intensivists should be prepared
for.
Case Series
Case 1
History and Examination
A 42-year-old man had a history of childhood cerebellar astrocytoma that had been
resected and treated with radiation. He subsequently developed hydrocephalus, requiring
placement of a ventriculoperitoneal (VP) shunt. During adulthood, he developed a right
temporoparietal meningioma, which recurred despite multiple resections and Gamma Knife
radiosurgery. During the admission of interest, he presented with progressive hearing
loss and regrowth of the meningioma ([Fig. 1A]).
Fig. 1 (A) Axial image slice from a CT head study (with contrast) of findings of a radiation-associated
meningioma in a 42-year-old man. This slice demonstrates extensive meningeal thickening,
enhancement, and nodularity in a 7-cm diameter portion of the right temporoparietal
convexity, suggestive of a recurrent meningioma. (B) Axial image slice from MRI brain study (contrast T1) postoperatively, 31 days later,
showing postoperative changes without residual enhancing nodular soft tissue, suggestive
of gross total resection of the meningioma. (C) Axial image slice from CT head study, an additional 9 days later, showing new multicompartment
pneumocephalus in bilateral ventricles, the right posterior fossa postoperative cavity,
right subdural spaces, and extension to the epidural space, as well as suprasellar
cistern air and new hydrocephalus. (D) Axial image slice from CT head, an additional 4 days later, showing resolution of
pneumocephalus, improvement of hydrocephalus, and new postoperative changes of closure
of the right external auditory canal and a tympanomastoid obliteration with removal
of the existing large cranioplasty mesh and removal and replacement of the free flap.
CT, computed tomography.
Operation and Perioperative Course
He underwent resection of this meningioma via a retrolabyrinthine approach and a wide
temporoparietal craniotomy, scalp resection and reconstruction with a vastus lateralis
flap, and shunt externalization ([Fig. 1B]). Postoperatively, he developed right CSF otorrhea, which was thought to be originating
from a small laceration of the right external auditory canal. The otorrhea persisted
despite maximal medical management. Ten days after the procedure, his mental status
declined, and repeat imaging demonstrated ventriculomegaly due to intraventricular
pneumocephalus ([Fig. 1C]). The patient was intubated, a lumbar drain was placed, and a blind closure of the
right external auditory canal and a tympanomastoid obliteration was performed with
the removal of the existing large cranioplasty mesh and removal and replacement of
the free flap ([Fig. 1D]). Later, he underwent internalization of his VP shunt and was discharged to rehabilitation.
Case 2
History and Examination
A 65-year-old man who underwent transnasal endoscopic resection of a large clival
meningioma with subsequent placement of an abdominal fat graft, Surgicel (oxidized
regenerated cellulose; Ethicon, Inc., Raritan, NJ), Duragen (porous collagen matrix;
Integra LifeSciences, Princeton, NJ), and then DuraSeal (polyethylene glycol hydrogel,
Ethicon, Inc.) were used to seal the large defect at his skull base. However, after
discharge at home, he expectorated the graft. He presented the following day with
CSF rhinorrhea and a severe headache, but no focal neurological findings. A CT of
his head showed significant free air intracranially along the frontal lobes, Sylvian
fissures, and in the lateral ventricles ([Fig. 2A, B]).
Fig. 2 (A, B) Axial and sagittal slices, respectively, from a CT sinus study of a 65-year-old
man who underwent transnasal endoscopic resection of a large clival meningioma with
subsequent placement of a fat graft and multilayered closure. He unfortunately expectorated
his fat graft and developed CSF rhinorrhea and severe headache. These slices show
postoperative material in the sphenoid sinus and along the posterior wall of the clivus
in the area of the resected tumor, as well as a large amount of air in the Sylvian
fissures and ventricles. (C) Axial image slice from CT head study 3 days later showing near resolution of cisternal
air, with a small amount of air remaining in the Sylvian fissures and frontal horns
of the lateral ventricles. (D) Axial image slice from a CT head study, an additional 10 days later, showing interval
right frontal ventricular catheter placement. CSF, cerebrospinal fluid; CT, computed
tomography.
Operation and Perioperative Course
He was maintained on cyclic oxygen therapy, which resulted in considerable improvement
of the pneumocephalus ([Fig. 2C]). Later, a lumbar drain was placed, and his skull base defect was repaired with
a new fat graft placement and bioabsorbable plating done via a revision transsphenoidal
approach. (While the technique of plating is now considered controversial due to the
increased risk of infection and the difficulty of revision surgery, it remains an
infrequently used option in refractory cases.[11]) Postoperatively, his course was complicated by a concern of infection, for which
he completed a course of empiric antibiotics. He was unable to wean from the lumbar
drain without leak recurrence; thus, a VP shunt was placed ([Fig. 2D]). One week after shunt placement, he was discharged home.
Case 3
History and Examination
A 75-year-old female had a history of spontaneous left sphenoid CSF leak and meningitis.
This leak was initially repaired endoscopically with a nasoseptal flap[12] ([Fig. 3A]). However, 1 week after discharge, she began to experience severe headaches with
altered mental status. Imaging performed suggested tension pneumocephalus and flap
failure ([Fig. 3B]).
Fig. 3 (A) Axial image slice from preoperative MRI brain study (T2 sequence) showing scattered
pneumocephalus along the falx and left frontal lobe, without significant mass effect
in a 75-year-old female with a spontaneous left sphenoid CSF leak and meningitis.
(B) Axial image slice from a postoperative CT head study, 16 days later, showing a large
amount of intracranial air exerting a mass effect on the frontal and temporal lobes
bilaterally. This is the classic “Mt. Fuji” sign of massive tension pneumocephalus.
CSF, cerebrospinal fluid; CT, computed tomography.
Operation and Perioperative Course
A burr hole was placed emergently at the bedside in the ICU using a cranial access
kit (commonly used with bedside ventricular drain placement), and a revision flap
reconstruction was performed in the operating room. Postoperatively, her mental status
did not improve despite empirical antibiotic treatment for suspected meningitis. A
repeat CT scan redemonstrated worsening pneumocephalus. Given this recurrent leak
after a prolonged period, it was believed that intracranial hypertension was causing
breakdown of her closure and most likely caused her original leak. She underwent a
second repair of the nasoseptal flap with lumbar drain placement. Postoperative imaging
initially demonstrated decreasing pneumocephalus; however, she later again developed
recurrent CSF leak a third time, and symptomatic pneumocephalus. She returned to the
operating room for a third repair and placement of a VP shunt, as it was suspected
that the LP shunt likely failed. She was ultimately discharged on long-term antibiotics
for suspected meningitis, but with resolution of the CSF leak and pneumocephalus.
Discussion
The Monroe-Kellie doctrine states that the sum of the volumes of the brain, CSF, and
blood within the adult cranial cavity is nearly[13] constant, and that a decrease in one necessitates an increase in one or more of
the other two, and vice versa.[14]
[15]
[16]
[17] In certain pathological cases, this compartment accommodates a fourth: Gas. The
physical distribution of gas within the cranial vault depends on the buoyant physics,
as air is less dense than fluid and hence brain matter. For example, this results
in the characteristic “Mt. Fuji” sign in the case of a tension pneumocephalus with
the air shifted anteriorly and superiorly in the supine patient (see [Fig. 3A]).[18]
The vast majority[9] of open intracranial procedures result in a small residual volume of air being entrapped
inside the surgical cavity, but these collections generally resolve spontaneously
and rarely lead to persistent clinical symptoms unless large. In the postoperative
patient, in addition to this air left in situ at the time of surgery, residual ambient–CSF
communication or resultant or preexisting fistulae can let air entrain (or certain
anesthetic gases by subsequent exchange) in any of the meningeal layers or inside
the brain parenchyma or within the ventricles.[18]
[19]
[20]
[21] Increased risk in the sitting position for more extensive pneumocephalus is described,
although the magnitude and clinical significance of this is probably low.[22]
[23]
[24] The majority of clinically significant or symptomatic pneumocephalus cases are due
to temporal region or transnasal skull base operations that lead to open communication
with the atmosphere and intracranial space (though it is the authors' opinion that
the incidence of symptomatic pneumocephalus has greatly decreased in the era of routine
placement of nasoseptal flaps[12]
[25] in anterior skull base reconstruction). Pneumocephalus after large-volume lumbar
puncture drainage in patients with elevated pressures or spinal anesthesia has also
been described.[26]
[27] Rare cases of symptomatic pneumocephalus have been described after VP shunt placement
secondary to an insidious congenital otic[28] or sinus defect.[29]
Symptoms of clinically significant pneumocephalus are primarily due to the mass effect
imposed by the gas on the brain matter, including headaches, nausea, vomiting, altered
sensorium, focal neurological deficits, seizures, and, in severe cases, coma and death
secondary to herniation from a large gas collection in tension pneumocephalus. The
clinical presentation is similar to other causes of elevated ICP or non-communicating
hydrocephalus. Small collections of sterile pneumocephalus are generally asymptomatic,
although air in the cranium can cause mild neurological symptoms even when not under
pressure, such as lethargy, confusion, and headache (though these non-specific symptoms
are often seen postcraniotomy in the absence of significant air). Untreated, these
symptoms generally resolve in 1 to 3 days as the bulk of the air is resorbed into
the circulation, though complete resolution may take weeks.
This diagnosis is made easily on CT imaging by identifying voxels of a region with
Hounsfield units of −1,000 (see [Figs. 1C], [2A], and [3B]) in the epidural and subdural spaces. Moderate and large collections are also easily
seen on cranial plain films due to the lucency and sharp borders created by the air–tissue
interface, though this is essentially a historical footnote at this point. Pneumocephalus
can also enter the subarachnoid space if introduced iatrogenically, with cases describing
cranial spread from air inadvertently introduced in the spine.[30] After evacuation of chronic subdural hematoma or resection of a large tumor, a large
benign pneumocephalus may be difficult to distinguish from a tension pneumocephalus
radiographically if the brain has yet to re-expand to occupy the residual intracranial
space.[18]
[20]
[31] In any case, with comparison to preoperative images, the presence of a midline shift
or imaging signs of herniation indicates the potential need for emergent treatment.
Historically, the use of nitrous oxide (N2O) after the beginning of surgical closure was also associated with tension pneumocephalus
due to the high solubility of nitrous oxide in the absence of ball-valve physiology.
This can lead to a pressurized pneumocephalus due to the increased pressure caused
by the equimolar exchange of nitrous oxide for the nitrogen gas in air, as the gas
will enter gas-filled spaces at least 30 times faster than nitrogen gas can exit.[32] Cases have been described of mass effect from nitrous oxide use in the sitting position,
even with discontinuation of nitrous oxide prior to wound closure, as the volatile
gas exchanges for air that is trapped in the cerebral convexities from CSF that had
drained out. This is a unique set of circumstances that can create life-threatening
tension physiology even without continued air entrainment or a one-way tissue valve.[33]
[34] These collections are ultimately self-limited once administration of the gas is
ceased (as nitrous oxide is rapidly cleared after its administration is stopped),
but injuries have been described due to the transient mass effect, which can be substantial.
New foci of intracranial air can be seen postoperatively either due to deep surgical
site infection or from contiguous infection from the nasal sinuses or mastoid, though
these are seen in a distinct imaging pattern and time course postoperatively. Infectious
causes of pneumocephalus are analogous to gas gangrene in other organ systems and
are generally due to Staphylococcus sp., Clostridium sp., and anaerobic Streptococcus sp., and are often due to traumatic or iatrogenic inoculation.[4] Other gas-producing organisms can rarely cause pneumocephalus, including Klebsiella sp. in a diabetic. Rarely, neoplasms, especially osteomas, epidermoid tumors, and
pituitary tumors, are associated with penetration of the dura with CSF leaks into
the sinuses, Eustachian tubes, or external auditory canal, including delayed presentations
associated with radiotherapy after resection.[35]
[36]
[37]
[38]
[39]
Management
Small collections of residual air without continued air entrapment or tension physiology
can then be observed. If there is sufficient clinical concern or if the lesion is
suspected to be symptomatic, bed rest and high concentrations of inspired oxygen for
up to 24 hours[40]
[41] and serial imaging. With high concentrations of supplemental oxygen, the displacement
of nitrogen by oxygen in the blood leads to an increased gradient of nitrogen in the
pneumocephalus as compared with circulation, which increases the net rate of dissolution
approximately two-fold due to mass action as well as intralesional exchange with the
more soluble oxygen.[40] Due to the pulmonary toxicity[41] of high inspired concentrations of oxygen, treatment should be suspended after 24 hours
and only repeated, or “cycled” as necessary thereafter, after a sufficient hiatus.
A finding of a collection larger than the surgical void or one that increases progressively
in size should be concerning for a complex lesion where air is being continuously
trapped into the wound by a one-way ball-valve formed by tissue or layers of dura
or closure material. If imaging after an acute change in mental status or development
of a focal deficit shows a large expanding collection of gas, this can be emergently
temporized at the bedside by twist-drill evacuation and optionally placement of a
ventricular catheter into the space (as opposed to the ventricle itself), open to
a collection system or bag, or percutaneous aspiration can be performed through an
existing cranial defect in the operative wound if possible. Emergent surgery can be
performed to evacuate the pneumocephalus when indicated and to correct the underlying
defect. In the case of recent transnasal skull base or sinus surgery, or middle fossa
surgery, early intubation may be useful to reduce pharyngeal air pressure and the
Venturi effect caused by ventilation past the defect. It may also be required if the
mental status of the patient is sufficiently depressed or there is concern about airway
protection. Infectious causes must be ruled out if suggested by laboratory or imaging
findings, or clinical history, though large collections would be uncommon. When intracranial
infection is a diagnostic possibility and is a potential cause of the gas collection,
the need for source control of the infection must be determined, and appropriate targeted
or empirical antibiotic therapy instituted.
If sudden deterioration and imaging findings of a large pneumocephalus are associated
with the recent placement of a lumbar or external ventricular drain, consider clamping
the drain, as it could be providing negative pressure, which could be drawing fluid
past a one-way valve through an iatrogenic or congenital dural defect.[26] This is only pertinent under clinical circumstances where use of the drain appeared
to trigger the clinical decline, as a functioning drain may be instrumental in controlling
ICP and successful CSF leak repair in other cases.
The use of adjunctive closure materials such as harvested abdominal fat, oxidized
cellulose polymer, and collagen or bovine pericardial dural patches has also been
shown to be helpful in closing large dural defects, and in refractory cases, the use
of these materials in repeated layers appears to be beneficial. Diversion of CSF with
lumbar drains may aid in closure and healing of the leak site, and is almost always
indicated in cases of intracranial hypertension[42] and multiply recurrent CSF leak or recurrent symptomatic pneumocephalus (though
note that recent evidence[43]
[44]
[45] suggest little value and potential harm from a prophylactic placement of lumbar
drains in transnasal neurosurgery in general). Acetazolamide can also be used for
weeks to months after repair of a leak when there is suspicion of idiopathic intracranial
hypertension (IIH)[46]
[47] to allow healing prior to confirmatory diagnosis of IIH, and a role for this agent
has been established for first-line treatment of this condition in combination with
weight loss.[48]
[49] Spontaneous CSF leaks have the highest recurrence rate of any leak,[50] and attention to sound closure (with a pedicled tissue flap[51] when possible) and management of intracranial hypertension if present is essential
for sustained results. Broad-spectrum antibiotic prophylaxis should be considered
and is often used routinely after postoperative CSF leaks, though evidence of benefit
is inconclusive in promptly repaired leaks.[52]
[53]
[54]
[55]
Though definitive guidelines do not exist, non-invasive positive pressure ventilation
should be held in the immediate period after transnasal surgery or any neurosurgery
where the anterior skull base is violated. The experience at our institution is that
a period of withholding continuous positive airway pressure (CPAP) for 7 days is sufficient
to minimize the risk of CSF leak and pneumocephalus when a vascularized pedicled flap
is used, such as a nasoseptal flap, in wound closure. Other authors have drawn similar
conclusions.[7]
[8]
[Figure 4] summarizes the management considerations and approaches discussed here.
Fig. 4 A suggested algorithm for the management of pneumocephalus. See the associated discussion
in the “Management” section of the text. CT, computed tomography.
Conclusion
Most intracranial air observed on postoperative imaging is expected; however, when
the amount of air is disproportionate to the wound bed, increases in volume, or becomes
symptomatic, emergent intervention may be necessary. Managing complex or tension cases
can often require multiple revision surgeries or procedures and a multidisciplinary
approach to minimize the risk of significant morbidity. Fortunately, advancements
in surgical techniques have significantly reduced the incidence of severe or symptomatic
cases of this complication.
